Introduction

Posterior canal dehiscence is an uncommon inner ear disorder in which the bony wall overlying the posterior semicircular canal is partially or completely absent. It belongs to a group of conditions known as third mobile window syndromes, which also includes the better-known superior canal dehiscence. The abnormal opening creates an additional route for sound and pressure to influence the perilymph and endolymph compartments, resulting in vestibular and auditory symptoms that can mimic more common disorders such as Ménière's disease, otosclerosis, or benign paroxysmal positional vertigo.

Because posterior canal dehiscence is rare, it may be overlooked during routine evaluation. The aim of this case report is to highlight the typical presentation, diagnostic workup and management of the condition. This is the first case in a planned series.

Case Presentation

A 42-year-old woman presented with an 18-month history of persistent disequilibrium and short episodes of vertigo provoked by loud sounds, straining, and bending forward. She described a sensation of pressure inside the affected ear and noted that her own voice sounded unusually loud in that ear. There was no history of head trauma, ear infection, or ear surgery. Otoscopy revealed normal tympanic membranes bilaterally. Neurological examination was unremarkable apart from a subtle down-beating and torsional nystagmus elicited by loud tone bursts delivered to the left ear. This finding was consistent with a positive Tullio phenomenon. Pressure application to the tragus also induced brief vertigo and nystagmus, a positive Hennebert sign. No spontaneous or positional nystagmus was observed in the dark.

Investigations

Pure-tone audiometry demonstrated a mild low-frequency conductive hearing loss in the left ear, with an air-bone gap of approximately 15 to 20 dB at 250 and 500 Hz. The right ear was normal. Tympanometry showed normal middle ear pressure and compliance on both sides. Stapedial reflexes were preserved.

Vestibular evoked myogenic potential testing revealed markedly reduced click thresholds for the cervical response on the left side, together with an enlarged ocular vestibular evoked myogenic potential amplitude. These findings supported the presence of an abnormally mobile third window.

High-resolution computed tomography of the temporal bone was performed with 0.5 mm collimation and multiplanar reconstruction angled to the plane of the posterior semicircular canal. The scans demonstrated a 3.2 mm area of absent bone over the posterior semicircular canal on the left side, consistent with posterior canal dehiscence. The superior semicircular canal was intact on both sides, excluding superior canal dehiscence.

Diagnosis

The diagnosis was left posterior canal dehiscence. The differential diagnosis included superior canal dehiscence, perilymphatic fistula, otosclerosis, Ménière's disease, and persistent postural-perceptual dizziness. The combination of sound- and pressure-induced vestibular symptoms, a low-frequency air-bone gap with normal tympanometry, lowered vestibular evoked myogenic potential thresholds, and characteristic computed tomography findings enabled a confident diagnosis.

Management and Outcome

Initial management was conservative. The patient received detailed counselling on trigger avoidance, including the use of ear protection in loud environments and avoiding Valsalva manoeuvres. She was advised to remain well hydrated and to avoid rapid changes in middle ear pressure. Six months after the diagnosis, her symptoms had improved considerably. The episodes of sound-induced vertigo were less frequent, and she no longer felt the need to restrict daily activities. Surgical options, such as posterior canal resurfacing or canal plugging via a transmastoid approach, were discussed in case symptoms became disabling, but the patient has not required surgery to date.

Discussion

Posterior canal dehiscence shares many clinical features with superior canal dehiscence. Both conditions result from an abnormal opening in the otic capsule that acts as a third mobile window. Sound and pressure stimuli can then produce inappropriate movement of endolymph, leading to vertigo, oscillopsia, and a characteristic low-frequency conductive hearing loss. The conductive component is thought to arise because the inner ear becomes more compliant, allowing sound energy to escape through the dehiscence rather than travelling normally through the cochlea.

In comparison with superior canal dehiscence, posterior canal dehiscence is less frequently recognised. Anatomically, the posterior semicircular canal lies close to the posterior fossa dura, and a dehiscence here creates a potential communication between the perilymphatic space and the cerebrospinal fluid. Although rare, this communication could theoretically increase the risk of bacterial meningitis, so accurate diagnosis is clinically relevant.

Imaging is essential for confirmation. Thin-slice computed tomography with oblique reformats along the plane of the posterior canal is the preferred method. However, because the normal thin bone overlying the canal can be subtle, the radiological finding must be interpreted together with the clinical picture and functional tests such as vestibular evoked myogenic potentials. Over-reliance on imaging alone may lead to overdiagnosis.

Conclusion

Posterior canal dehiscence should be considered in patients presenting with sound- or pressure-induced vertigo, positional symptoms, or an otherwise unexplained conductive hearing loss in the presence of a normal tympanic membrane. A structured evaluation that includes careful bedside testing, audiometry, vestibular evoked myogenic potentials, and high-resolution computed tomography of the temporal bone allows accurate diagnosis. Conservative management is effective in many cases, and surgery can be reserved for patients with severe, disabling symptoms.